We wish to determine: (a) how to stabilize ferroactivator so as to permit assays of its active form; (b) whether genetically diabetic animals have more ferroactivator in their gluconeogenic tissues than do normal animals; (c) whether increased rates of gluconeogenesis in diabetes are the result of enhanced ferroactivator activity; and (d) the exact mode of action of the ferroactivator in permitting Fe2ion to activate PEPCK.